The physiological response in the mammary gland to Escherichia coli infection reflects a conflict between glucose need for milk production and immune response

Abstract

30Upon entry into the mammary gland, mammary pathogenic strains of Escherichia 31 coli rapidly grow using milk as a nutrient source, in a manner highly dependent on the 32 expression of the ferric-dicitrate system by these bacteria. Intra-mammary challenge with 33 distinct mammary pathogenic E. coli (MPEC) strains result in development of clinical 34 acute mastitis, with peak bacterial counts in milk at 16-24 h post-challenged and profound 35 immune changes found in the milk. The main biochemical changes measured in milk 36 were partially in accord with lipopolysaccharide-induced mastitis, with increased 37 glucose-6-phosphate and lactate dehydrogenase activity or prolonged lactate 38 dehydrogenase, and Glu6P/Glu alterations. Changes also reflect physiological responses 39 to inflammation in the mammary gland, as in the balance between aerobic and anaerobic 40 metabolism (citrate to lactate ratios). Some alterations measured in milk resolved with 41 days after challenge but other remained for above one month, regardless of bacterial 42 clearance. The results suggest that E. coli mastitits can be divided into two stages: an 43 acute, clinical phase, as an immediate response to bacterial infection in the mammary 44 gland and a chronic phase, independent of bacteria clearance, and in response to the tissue 45 damage caused in the first phase. 46 47

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